Linked Life Data

10903405

Source:http://linkedlifedata.com/resource/pubmed/id/10903405

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-9-21
pubmed:abstractText
An outstanding problem in psychiatry concerns how to link discoveries about the pharmacological, neurophysiological, and neuroanatomical substrates of mental disorders to the abnormal behaviors that they control. A related problem concerns how to understand abnormal behaviors on a continuum with normal behaviors. During the past few decades, neural models have been developed of how normal cognitive and emotional processes learn from the environment, focus attention and act upon motivationally important events, and cope with unexpected events. When arousal or volitional signals in these models are suitably altered, they give rise to symptoms that strikingly resemble negative and positive symptoms of schizophrenia, including flat affect, impoverishment of will, attentional problems, loss of a theory of mind, thought derailment, hallucinations, and delusions. This article models how emotional centers of the brain, such as the amygdala, interact with sensory and prefrontal cortices (notably ventral, or orbital, prefrontal cortex) to generate affective states, attend to motivationally salient sensory events, and elicit motivated behaviors. Closing this feedback loop between cognitive and emotional centers is predicted to generate a cognitive-emotional resonance that can support conscious awareness. When such emotional centers become depressed, negative symptoms of schizophrenia emerge in the model. Such emotional centers are modeled as opponent affective processes, such as fear and relief, whose response amplitude and sensitivity are calibrated by an arousal level and chemical transmitters that slowly inactivate, or habituate, in an activity-dependent way. These opponent processes exhibit an Inverted-U, whereby behavior becomes depressed if the arousal level is chosen too large or too small. The negative symptoms are owing to the way in which the depressed opponent process interacts with other circuits throughout the brain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-3223
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
81-98
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The imbalanced brain: from normal behavior to schizophrenia.
pubmed:affiliation
Department of Cognitive and Neural Systems and Center for Adaptive Systems, Boston University, Boston, Massachusetts 02215, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review